| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2000: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
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| Research Abstract |
We studied experimentally using a spinal cord continuous compression model in rats to analyze the mechanism of chronic compression myelopathy. The rat thoracic spinal cord was epidurally pressured continuously with uterine-cervical dilator Dilapan, which has the character of slow expanding. The lesions were investigated morphologically, by histochemistry, electron microscopy, immunohistochemistry, as well as conventional histology for 1 days to 3 months..
Histologically, in acute stage (within 7 days), mildly necrotic changes of the spinal cord occurred, mostly localized in the pressured sites, however, no apparent hemorrhagic necrosis was observed. In the white matter, edema but not destructive changes were seen at 24 hours. The spongy change with axonal degeneration was prominent for 1-2 weeks, which were not localized at the compression site but distributed diffusely in the white matter, continuing for 3 months later. Histochemistry disclosed that the spongy change of white matter wa
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s associated with decrease of axons and myelin 2 weeks later. EM examinations demonstrated that main change in the lateral column was degeneration of axon of myelinated fibers, such as edematous swelling, myelintangles, detachment from myelin sheath, and demyelinated axons. These axonopathy and demyelinating changes had been continuously seen as long as 3 months. Immunnohistochemistry using monoclonal antibody, APC (Ab-7), specific antibody against oligodendrocytes, showed the decrease of the cell number after 1-week compression, and most prominent at 2-4 weeks. Furthermore, by TUNEL examination, TUNEL positive cells were observed in the white matter at 24-48 hours with peak at 72 hours.
Tease results indicate that our experimental model is suitable for the analysis of chronic compression myelopathy. The continuous axonopathy with demyelinating changes occurred in the white matter may be the main changes in compression myelopathy. Oligodendrocyte damage, probably due to apoptotic cell death, may cause demyelination of the remaining after continuous compression. Less
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